Snake venom is complex mixture of many substances with a wide spectrum of biological activities. Snake venom is a store house for numerous bioreactive components, such as toxins, enzymes, hormones and growth factors. Snake venom derived proteins have importance in medicine, pharmacology and various diagnostic procedures. The publication "Medical Use of Snake Venoms" by Kurt Stocker (1) reveals the state of the art.
The pioneering work of Sanders et al. (2) in the early fifties was the earliest reported study on the interaction of snake venom toxins and viruses. In 1958 the same authors (3) studied an antiviral effect of a snake venom neurotoxin in cell cultures and in animals. They demonstrated the inhibition of Semiliki Forest virus induced plaque formation by purified cobra venom neurotoxins. In 1977 the same authors (4) observed that venom neurotoxin interfered with the human strains of Poliomyelitis (Brunhild and Lansing) in Rhesus monkeys even after being chemically converted to a neurotoxoid.
In 1960 Anderson and Ada (5) observed that 100 .mu.g/ml of purified phospholipase A.sub.2 (PhA.sub.2) from Pseudechis porphyriacus venom rapidly decreased the infectivity titer of Murray encephalitis virus. In the following year, similar observations were reported by Dayton (6) for Rous Sarcoma and MH2 tumor viruses. Venom derived phospholipase A.sub.2 (enzyme name, phospatide acyl hydrolase) has several laboratory applications based on its ability to hydrolyze the acyl group on typical phoslipids of a cell membrane. However, phospholipase A.sub.2 from various snake species differs substancially in molecular weight and activity.
Newcastle disease virus contains a "fusion factor" which causes animal cells to fuse. In 1967 Kohn (7) observed that this fusion was blocked by PhA.sub.2 purified from Hydrophis haemachatus and Vipera palestinae venoms, although the hemagglutin, hemolysin and neuraminidase properties of the virus were not affected. Furthermore, in 1974 Wallstrom et al. (8) reported that PhA.sub.2 from Naja nigricolis venom partially disrupted the envelop of influenza virus.
It is clear from the literature that snake venom proteins have been tested for their antiviral properties. Beginning two decades ago, venoms were tested on a limited scale but only for a few viruses, which were mostly RNA viruses. Furthermore, phospholipase A.sub.2 from various species of snake venoms have shown antiviral activity on RNA viruses. The presence of numerous different proteins in typical snake venom suggests that there may also be antiviral factors for DNA viruses, specifically for herpes viruses. According to Meier (10), "Very interesting substances in snake venoms are waiting to be discovered".
Herpes simplex viruses type 1 and type 2 are double stranded DNA viruses. The clinical entities attributable to herpes virus type 1 include the following. (1) Acute herpetic gingivostomatitis which occurs mostly in small children. (2) Eczema herpeticum--Kaposi's varicelliform eruption. In this illness, there may be extensive vesiculation of the skin over much of the body and high fever. In rare instances the illness may be fatal. (3) Keratoconjunctivitis infection of eye. With recurrent infection there may be progressive involvement of the corneal stroma with permanent opacification and blindness. (4) Herpes encephalitis--carries a high mortality rate and survivers often have residual neurologic defects. (5) Herpes labialis--cold sores is the most common recurrent disease in the form of oral lesions.
Herpes virus type 2 is implicated in the following: (1) Genital herpes herpes progenitalis is characterized by vesiculoulcerative lesions of the penis of the male or the cervix, vulva, vagina and perineum of the female. (2) Neonatal herpes-herpes type 2 may be transmitted to the newborn during birth by contact with herpetic lesions in the birth canal producing permanent brain damage.
Varicella--zoster virus is a double stranded DNA virus and is morphologically identical with herpes simplex viruses. Herpes zoster--commonly known as shingles is a sporadic incapacitating disease of adults, rare in children, which is characterized by an inflammatory reaction of the posterior nerve roots and ganglia, accompanied by the affected sensory nerves.